Recent studies have shown that mediators of inflammation, useful in predicting risk of developing cardiovascular disease in healthy asymptomatic individuals, are also increased by experimental sleep deprivation. Low basal increases in inflammatory markers are also seen in "metabolic syndrome" and we hypothesize that inadequate or insufficient sleep may be a pivotal contributing factor in the development of metabolic syndrome. We will test the hypothesis that basal changes in inflammation are actually secondary to cardiovacular factors associated with shear stress, by blocking the increase of blood pressure that is known to ensue during sleep deprivation. We expect that blocking the sleep deprivation associated increase in blood pressure will prevent the rise of inflammatory markers. We will also test the hypothesis that moderately adipose individuals are at greater risk to suffer the inflammatory and autonomic consequences of acute sleep deprivation. In screening data from this study we will also investigate the relationship between adiposity, cardiovascular fitness, C-reactive protein and habitual sleep duration and quality.